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题名:SIGNAL TRANSDUCTION AND NUCLEAR RESPONSES IN STAPHYLOCOCCUS AUREUS-INDUCED EXPRESSION OF HUMAN {beta}-DEFENSIN-3 IN SKIN KERATINOCYTES.
作者:Menzies BE, Kenoyer A.
来源:Infect Immun. 2006 Sep 5; [Epub ahead of print]
URL :http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16954397&query_hl=4&itool=pubmed_docsum
日期:060930
摘要:The human beta-defensin-3 (hBD-3) is an inducible epithelial peptide antibiotic that has potent anti-staphylococcal activity. Infection of skin epithelial cells with viable Staphylococcus aureus, a common skin pathogen, induces increased gene expression of hBD-3 and other antimicrobial peptides. The aim of this study was to identify signaling pathways and nuclear responses that contribute to the gene expression of hBD-3 in primary human keratinocytes upon contact with S. aureus. Increased hBD-3 peptide was observed by immunofluorescence microscopy in keratinocytes exposed to S. aureus and to lipoteichoic acid (LTA). Both are ligands for the cell surface Toll-like receptor-2 (TLR2) and thus, the contribution of TLR2 signaling in hBD-3 expression was examined. Functional inhibition of TLR2 prior to S. aureus stimulation significantly decreased hBD-3 mRNA levels by 37%, attesting to the involvement of this surface receptor in the initial recognition and downstream signaling for hBD-3 expression. Treatment of keratinocytes with a p38 mitogen-activated protein kinase (MAPK) inhibitor prior to either S. aureus or LTA stimulation was associated with reduced hBD-3 mRNA transcripts and peptide. We also propose a role for the MAPK-regulated transcriptional activating protein -1 (AP-1) in S. aureus-induced hBD-3 gene expression. Combined, these studies indicate a role for TLR2 signaling and MAPK activation in the up-regulation of hBD-3 and demonstrate the innate immune capacity of skin keratinocytes under conditions of S. aureus challenge to enhance the local expression of this anti-staphylococcal peptide antibiotic.

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